ANIMAL FEED SCIENCE AND TECHNOLOGY
·
2025
·
IF 2.7
Weijun Chen,Shiyang Gao,Ping Sun,Lei Han,Zhenyang Zhang
The investigation was to validate the alleviating effect of sodium butyrate on high-fat diet-induced gut injury and growth inhibition in largemouth bass ( Micropterus salmoides ). Five diets were designed: four high-fat diets (18 % crude lipid) supplemented with sodium butyrate at 0 % (HF), 0.05 % (HFS1), 0.1 % (HFS2), and 0.2 % (HFS3), as well as a control diet (C, 10 % crude lipid). Three tanks (30 fish each tank) were randomly allocated to each diet. Fish (4.0 g) were fed to apparent satiation for sixty days. Results indicated that HF dramatically reduced fish growth and induced oxidative stress, mucosal barrier dysfunction, gut inflammation, and gut dysbiosis compared to C. However, in comparison to HF, HFS1, HFS2, and HFS3 diets significantly promoted feed intake and weight gain rate, relieved oxidative stress by increasing antioxidant defense (e.g., total superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione, and nuclear factor E2-related factor 2) and reducing malondialdehyde content, enhanced mucosal barrier by upregulating the expression of occludin, mucin3a, zona occluding-1, hypoxia-inducible factor-1α, and lysozyme, and reduced inflammation by downregulating the expression levels of interleukin 1β and tumor necrosis factor α ( P < 0.05). Moreover, HFS1 and HFS3 dramatically reduced Tenericutes and Mesomycoplasma abundance, whereas HFS1 increased Lactococcus abundance when compared to HF ( P < 0.05). Correlation analysis revealed a significant relationship between fish growth and gut injury with mucosal barrier proteins and gut microbiota (e.g., Tenericutes, Mesomycoplasam , and Lactococcus ) ( P < 0.05). These findings suggested that sodium butyrate can help mitigate the detrimental effects of high-fat diets on fish growth and gut health.
研究领域:
水产养殖学
·
营养学
·
微生物学
✓ 已验证
产品关联
DOI
高影响因子
FOOD CONTROL
·
2021
·
IF 5.548
Wenxiu Zhu,Jingzhu Gao,Hongli Liu,Jiaxiu Liu,Tong Jin,Ningbo Qin,Xiaomeng Ren,Xiaodong xia
Vibrio parahaemolyticus ( V. parahaemolyticus ) is an important foodborne pathogen , which is frequently associated with seafood consumption and commonly causes gastroenteritis. The biofilm formed by V. parahaemolyticus in the food production chain poses a continuous threat to food safety, therefore effective antibiofilm strategy is in urgent need. Sodium butyrate is widely used in food, feed, cosmetics and other industries, and could be used as a flavoring agent in food as well as a dietary supplement for health. This study aims to examine the antibiofilm effect of sodium butyrate against V. parahaemolyticus. We found that sodium butyrate could inhibit biofilm formation at subinhibitory concentrations (SICs). Microscopic images coupled with extracellular polysaccharide quantification showed that V. parahaemolyticus biofilm was loosely structured with fewer biofilm constituents when treated with sodium butyrate. XTT reduction assay illustrated that sodium butyrate interfered with the metabolic activity of cells encased inside biofilm and decreased their viability. Sodium butyrate decreased the motility and surface hydrophobicity of V. parahaemolyticus , and interfered with quorum sensing by using two reporter strains. The RT-qPCR analysis revealed that sodium butyrate down-regulated genes associated with biofilm formation. These findings suggest that sodium butyrate has the potential to be developed as a potent agent against V. parahaemolyticus biofilm in food industries.
研究领域:
微生物学
·
食品科学
✓ 已验证
产品关联
DOI
高影响因子
Journal of Clinical and Translational Hepatology
·
2024
·Vol. 13
·期 2
·105
·
IF 3.1
Yimeng Zhou,Yang Ding,Yanwei Li,Qiuju Sheng,Chao Han,Yaoxin Fan,Ziyi Wang,Bingchao Lu,Xiaoguang Dou,Chong Zhang
Background and Aims Necroptosis is critical for regulating intestinal epithelial cells (IECs). Butyric acid (BA), produced during intestinal microbial metabolism, protects the intestinal epithelial barrier. However, whether necroptosis occurs in IECs during liver cirrhosis and whether sodium butyrate (NaB) can regulate necroptosis have not yet been reported. In this study, we aimed to investigate whether IECs undergo necroptosis in cirrhosis and whether NaB can regulate necroptosis and the related regulatory mechanisms. Methods Serum levels of RIPK3, MLKL, and Zonulin, as well as fecal BA levels, were measured and correlated in 48 patients with liver cirrhosis and 20 healthy controls. A rat model of liver cirrhosis was established, and NaB was administered. The expressions of MLKL, p-MLKL, and tight junction proteins were measured. We conducted an in vitro investigation of the effect of NaB on necroptosis in the HT29 cell line. Results Serum levels of RIPK3, MLKL, and Zonulin in the liver cirrhosis group were higher, while fecal BA levels were lower than those in the control group. Zonulin levels were positively correlated with RIPK3 and MLKL levels, while fecal BA levels were negatively correlated with serum MLKL levels, but not with RIPK3 levels. NaB reduced the mRNA and protein expression of MLKL but had no effect on RIPK1 and RIPK3 in vitro. Rescue experiments demonstrated that NaB inhibited necroptosis through E2F1-mediated regulation of MLKL. Conclusions NaB alleviates intestinal mucosal injury and reduces necroptosis in IECs in liver cirrhosis. It also inhibits the necroptosis of IECs and protects the intestinal barrier by reducing E2F1 expression and downregulating MLKL expression levels. These results can be employed to develop a novel strategy for treating complications arising from liver cirrhosis.
研究领域:
医学
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消化系统疾病
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分子生物学
✓ 已验证
DOI
PubMed
高影响因子
JOURNAL OF FOOD BIOCHEMISTRY
·
2022
·Vol. 46
·期 10
·e14334
·
IF 3.654
Xue Tang,Yongjuan Sun,Yingrui Li,Shuhua Ma,Kai Zhang,Ailing Chen,Yipin Lyu,Renqiang Yu
Sodium butyrate (NaB), obtained by fermenting dietary fiber via intestinal microflora, was recently shown to improve the activity of some antioxidant enzymes in vivo. This study aims to investigate the term changes of mitochondrial energy metabolism and redox homeostasis in skeletal muscles and clarify the regulatory mechanism and dose effect of NaB on skeletal muscle. Male Sprague–Dawley rats were divided into the control group, obesity-prone (OP) group and obesity-resistant (OR) group based on the gain of body weight after 8 weeks' of feeding high-fat diet (HFD), followed by sacrificing rats at the end of 20th week. NaB intervention (12 weeks) could effectively reduce the body weight of rats in the OP and OR groups. NaB also mediated upregulation of antioxidant enzyme activity and GSH/GSSG ratio, while reducing reactive oxygen species (ROS) levels and malondialdehyde (MDA) content. At the molecular level, NaB upregulated Pi3k , Nrf2 , Nqo-1 , and Ho-1 , but downregulated Gsk-3β mRNA expression by regulating the Nrf2 antioxidant pathway to enhance tissue antioxidant capacity. At the same time, NaB intervention significantly upregulated Glut4 , Irs-1 , Pdx1 , and MafA , expression in gastrocnemius muscles of OP and OR rats, and elevated insulin secretion and muscle insulin sensitivity. Thus, NaB activates antioxidant pathway, improves the antioxidant capacity of obese rat tissues and promotes glucose metabolism. Practical applications This study found that obesity-prone and obesity-resistant rats have differences in mitochondrial redox homeostasis and energy metabolism in tissues. Meanwhile, sodium butyrate can effectively promote muscle protein synthesis, increase insulin sensitivity, and promote glucose metabolism in obesity rats. Thus, sodium butyrate supplementation or increasing intestinal butyrate production (e.g., by consuming foods rich in dietary fiber) is a potential means of improving the body's glucose metabolism and obesity profile.
研究领域:
营养学
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代谢学
·
分子生物学
·
药理学
·
内分泌学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Frontiers in Pharmacology
·
2021
·
IF 5.811
Zhou Haikang,Li Guoqing,Wang Yang,Jiang Rendong,Li Yicheng,Wang Huhu,Wang Fei,Ma Hairong,Cao Li
Osteoarthritis (OA) is a degenerative joint disease with multiple etiologies that affects individuals worldwide. No effective interventions are currently available to reverse the pathological process of OA. Sodium butyrate (NaB), a component of short-chain fatty acids (SCFAs), has multiple biological activities, including the attenuation of inflammation and anti-tumor activities in various diseases. However, whether the protective effects of NaB in OA are associated with the promotion of autophagy had not been investigated. Here, we explored the chondroprotective properties of NaB in an interleukin (IL)-1β-induced inflammatory chondrocyte model and an anterior cruciate ligament transection (ACLT) mouse model. Hematoxylin and eosin (HE), Safranin O, and immunohistochemical staining were performed to evaluate the effects of NaB treatment on articular cartilage. An optimal NaB dose for chondrocyte treatment was determined via cell counting kit-8 assays. Immunofluorescence and transmission electron microscopy were used to detect autophagy in chondrocytes. Flow cytometry was utilized to detect reactive oxygen species (ROS), cell cycle activity, and apoptosis in chondrocytes. Western blot and immunostaining were performed to evaluate the protein expression levels of relevant indicators. We found that the administration of NaB by oral gavage could attenuate cartilage degradation. In parallel, NaB treatment could enhance the activation of autophagy, increase autophagic flux, decrease extracellular matrix degradation, and reduce apoptosis by restraining inflammation, ROS production, and cell cycle arrest in IL-1β-treated chondrocytes. The protective effects of NaB could be partially abolished by the autophagy inhibitor 3-methyladenine (3-MA), which indicated that the protective effects of NaB against OA were partially governed by the enhancement of autophagy to restrain the formation of inflammatory mediators and ROS and regulate cell cycle progression and apoptosis in chondrocytes. In conclusion, NaB could attenuate OA progression by restoring impaired autophagy and autophagic flux via the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway, both in vitro and in vivo, implying that NaB could represent a novel therapeutic approach for OA.
研究领域:
风湿病学
·
药理学
·
分子生物学
·
病理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL POLLUTION
·
2025
·
IF 7.3
Ziyan Wang,Wei Zhang,Ziyan Liu,Danyang Huang,Huiwen Kang,Jingyu Wang,Guangyu Jiang,Ai Gao
BDE-209 has a causal relationship with adverse health outcomes. However, research on its effect on bone homeostasis is relatively lacking. This study examined the relationship between BDE-209 exposure and bone health, as well as the underlying mechanisms, using both in vitro and in vivo models. In animal studies, female SD rats were administered BDE-209 for 60 days. Bone mineral density, bone microstructure, gut microbiota, and inflammaging markers were measured. Furtherly, THP-1 cell-derived macrophages were treated with a culture medium containing population-relevant dose of BDE-209 or sodium butyrate. The expression of M1 macrophage markers, osteoclast markers, and inflammatory cytokines was measured. Then macrophages were induced by osteoclast conditioned medium to evaluate the effect of BDE-209 on their differentiation into osteoclasts. Results showed reduced humeral bone density, enhanced osteoclast activity, upregulation of IL-1β, TNF-α, IL-6, and activation of PGC-1α/NAD + /cGAS-STING in the exposed group. 16s sequencing revealed that BDE-209 disrupts the abundance of the gut microbiota, notably a reduction in Lachnospiraceae . In vitro, BDE-209 can stimulate macrophages to differentiate more osteoclasts and activate the cGAS-STING pathway, while sodium butyrate can inhibit these effects. This study reveals that gut microbiota dysbiosis is involved in BDE-209-induced bone homeostasis disorder through inflammatory aging and sodium butyrate can mitigate this effect. Overall, this study provides research data for the precaution and treatment of osteoporosis associated with BDE-209 exposure.
研究领域:
毒理学
·
免疫学
·
骨生物学
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微生物学
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药理学
✓ 已验证
DOI
PubMed
高影响因子
PSYCHOPHARMACOLOGY
·
2021
·Vol. 239
·期 1
·215-227
·
IF 4.53
Wang Chen,Zheng Dongpeng,Weng Fanglin,Jin Yongzeng,He Ling
Rationale Energy metabolism disorder is a widespread feature that exists in the early clinical stages of Alzheimer’s disease (AD). Astrocyte is the most numerous and the largest glial cell in the brain. By transporting energetic fuels such as lactate and ketones to neurons, astrocytes play a pivotal role in maintaining the cerebral energy homeostasis. Sodium butyrate (NaB), a type of short-chain fatty acid; its anti-inflammatory effect; and inhibition on histone deacetylases have been widely studied. Methods Spatial memory and cognitive ability of mice were assessed by using behavioral tests. Western blotting and ELISA kits were used to detect related protein levels and other biochemical markers, respectively. Objectives To prove the therapeutic effect of NaB on AD cognitive impairment and provide possible research ideas for mechanism exploration. Results Administration of NaB could improve the cognitive impairments induced by Aβ 25–35 in mice. Furthermore, NaB could promote the differentiation of astrocytes towards A2-neuron-protective subtype, astroglial mitochondrial function, and lactate shuttle between astrocytes and neurons. Conclusion These findings reveal the effect of sodium butyrate on astrocytes, which may improve the pathological status of AD and provide experimental basis for sodium butyrate treatment of AD.
研究领域:
神经科学
·
药理学
·
神经退行性疾病
✓ 已验证
DOI
PubMed
高影响因子
Journal of Functional Foods
·
2024
·
IF 3.8
Jinping Wang,Jianmin Wu,Zishen Lin,Ning Ma,Zhaoyue Men,Chao Zhang,Xi Ma,Hongyu Zheng
The invasion of pathogens derived from diet or the environment triggers intestinal inflammation, which is a result of the host intestinal barrier damage and immune dysfunction, such as the decrease of host defense peptides (HDPs) and inhibition of cell proliferation. Herein, the siRNA interference demonstrated that a critical lysozyme, which was mainly induced by dietary supplementations of sodium butyrate and forskolin, improved cell proliferation by inhibiting p38 MAPK and JNK signaling pathways and reinforced the intestinal barrier. Moreover, we established a mouse model of intestinal inflammation with Citrobacter rodentium ( C. rodentium ). It was found that NaBu and FSK stimulated intestinal epithelial proliferation to repair barrier damage, and performed stronger disease resistance to C. rodentium infection on account of the lysozyme upregulation in colon. Therefore, this study revealed that NaBu and FSK prevented or alleviated the development of foodborne infections by promoting lysozyme expression, which may be mediated by the effect of lysozyme on promoting cell proliferation and improving barrier function.
研究领域:
胃肠病学
·
免疫学
·
分子生物学
·
微生物学
✓ 已验证
产品关联
DOI
高影响因子
INFLAMMATION
·
2012
·Vol. 35
·期 5
·1676-1684
·
IF 1.747
Liu Tengfei,Li Jing,Liu Yuxin,Xiao Nan,Suo Haitao,Xie Kun,Yang Chunliu,Wu Chen
Short-chain fatty acids (SCFAs) produced by the colonic bacterial fermentation of dietary fiber contribute a significant proportion of daily energy requirement. Furthermore, these compounds are modulators of macrophage function and potential targets for the development of new drugs. The aims of this study were to evaluate the effects of three types of SCFAs (sodium acetate (NaAc), sodium propionate (NaP), and sodium butyrate (NaB)) on the production of NO and inducible nitric oxide synthase (iNOS) and proinflammatory and antiinflammatory cytokines (tumor necrosis factor-α (TNF-α) and interleukin (IL-1, IL-6, and IL-10)) and to observe the effect of NaAc on inhibiting lipopolysaccharide (LPS)-induced NF-κB activation in LPS-stimulated RAW264.7 cells. The results show that three types of SCFAs (acetate, propionate, and butyrate) reduced the production of proinflammatory factors, including TNF-α, IL-1β, IL-6, and NO, and inhibited the vitality of iNOS. Meanwhile, SCFAs enhanced the production of antiinflammatory cytokine IL-10 in lower concentrations (1–1,200 μmol/L). Like NaB, NaAC inhibited LPS-induced NF-κB activation. These results may hold promise on the role that SCFAs have on the prevention and treatment of various inflammatory conditions.
研究领域:
免疫学
·
药理学
·
细胞生物学
·
炎症研究
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Microbiology Spectrum
·
2021
·Vol. 9
·期 2
·
IF 7.171
Huidi Wang,Wei Song,Qiheng Wu,Xuxuan Gao,Jie Li,Chuhong Tan,Hongwei Zhou,Jiajia Zhu,Yan He,Jia Yin
The complication of type 2 diabetes (T2D) exacerbates brain infarction in acute ischemic stroke (AIS). Because butyrate-producing bacteria are decreased in T2D and butyrate has been reported to be associated with attenuated brain injury in AIS, we hypothesize that administering butyrate could ameliorate T2D-associated exacerbation of brain infarction in AIS. Therefore, we first validated that Chinese AIS patients with T2D comorbidity have significantly lower levels of fecal butyrate-producing bacteria and butyrate than AIS patients without T2D. Then, we performed a 4-week intervention in T2D mice receiving either sodium butyrate (SB) or sodium chloride (NaCl) and found that SB improved the diabetic phenotype, altered the gut microbiota, and ameliorated brain injury after stroke. Fecal samples were collected from T2D mice after SB or NaCl treatment and were transplanted into antibiotic-treated C57BL/6 mice. After 2 weeks of transplantation, the gut microbiota profile and butyrate level of recipient mice were tested, and then the recipient mice were subjected to ischemic stroke. Stroke mice that received gut microbiota from SB-treated mice had a smaller cerebral infarct volume than mice that received gut microbiota from NaCl-treated mice. This protection was also associated with improvements in gut barrier function, reduced serum levels of lipopolysaccharide (LPS), LPS binding protein (LBP), and proinflammatory cytokines, and improvements in the blood-brain barrier.IMPORTANCE Ischemic stroke is a major global health burden, and T2D is a well-known comorbidity that aggravates brain injury after ischemic stroke. However, the underlying mechanism by which T2D exacerbates stroke injury has not been completely elucidated. A large amount of evidence suggests that the gut microbiota composition affects stroke outcomes. Our results showed that the gut microbiota of T2D aggravated brain injury after ischemic stroke and could be modified by SB to afford neuroprotection against stroke injury. These findings suggest that supplementation with SB is a potential therapeutic strategy for T2D patients with ischemic stroke.
研究领域:
神经科学
·
药理学
·
微生物学
·
代谢疾病
✓ 已验证
DOI
PubMed
高影响因子
ENVIRONMENT INTERNATIONAL
·
2024
·
IF 10.3
Yunting Li,Anfei Liu,Kaiju Chen,Lifan Li,Xiaoshun Zhang,Fei Zou,Xingmei Zhang,Xiaojing Meng
Lead is an environmentally widespread neurotoxic pollutant. Although the neurotoxicity of lead has been found to be closely associated with metabolic disorders, the effects of short-chain fatty acids on the neurotoxicity of lead and its mechanisms have not yet been explored. In this study, the results of open field tests and Morris water maze tests demonstrated that chronic lead exposure caused learning and memory deficits and anxiety-like symptoms in mice. The serum butyric acid content of lead-treated mice decreased in a dose-dependent manner, and oral administration of butyrate significantly improved cognitive memory impairment and anxiety symptoms in lead-exposed mice. Moreover, butyrate alleviated neuroinflammation caused by lead exposure by inhibiting the STAT3 signaling in microglia. Butyrate also promoted the expression of acetyl-CoA synthetase ACSS2 in hippocampal neurons, thereby increasing the content of acetyl-CoA and restoring the expression of both histone H3K9ac and the downstream BDNF. We also found that the median butyric acid concentration in high-lead exposure humans was remarkably lower than that in the low-lead exposure humans (45.16 μg/L vs. 60.92 μg/L, P < 0.01), and that butyric acid significantly mediated the relationship of lead exposure with the Montreal cognitive assessment scores, with a contribution rate of 27.57 %. In conclusion, our results suggest that butyrate supplementation is a possible therapeutic strategy for lead-induced neurotoxicity.
研究领域:
神经科学
·
毒理学
·
药理学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Advanced Healthcare Materials
·
2024
·
IF 10
Yanwei Lv,Mengni Jiang,Yongliang Ouyang,Xiaoyi Zheng,Liang Zhang,Jinpeng Yao,Lianghao Hu,Jiulong Zhao,Zhaoshen Li,Shige Wang
Intestinal barrier dysfunction is related to diseases such as inflammatory bowel disease (IBD) and severe acute pancreatitis (SAP). Butyrate and its derivatives (e.g., sodium butyrate (SB)) can alleviate gut inflammatory responses. Nevertheless, these substances usually cannot fully exert protective effects due to low bioavailability. This research aimed to offer microspheres for treating intestinal barrier injury. Sodium alginate solution is prepared to dissolve SB, followed by mixing with chitosan (CS)-protocatechuic aldehyde (PA)/calcium chloride solution. The required CS-PA/calcium alginate/SB (CPC/SB) microspheres are formed in this manner. Subsequently, the therapeutic effects of CPC/SB microspheres on intestinal barrier injury through in vivo dextran sulfate sodium salt (DSS)-induced IBD and sodium taurocholate (STC)-induced SAP models is explored. Results: The CPC/SB microspheres exhibited excellent antioxidant properties. In vivo bioluminescence imaging experiment confirmed the microspheres effectively targeted the inflammatory gut in IBD. Further in vivo experimental results indicated the microspheres significantly repaired intestinal barrier damage, exerting protective effects in IBD and SAP. Additionally, 16S rDNA sequencing explained the microspheres can regulate the balance between harmful and beneficial bacteria (such as Alistipes, Odoribacter, and Rikenellaceae RC9). This study provides a possible synthetic strategy of microsphere carriers to serve as a potential therapeutic tool for intestinal barrier injury.
研究领域:
药学
·
胃肠病学
·
生物技术
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
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